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Bacteria Could Contribute To Development Of Wound-Induced Skin Cancer

﻿Researchers have identified a new mechanism by which skin damage triggers the formation of tumours, which could have important therapeutic implications for patients suffering with chronic ulcers or skin blistering diseases.

The study, published in Nature Communications, highlights an innate sensing of bacteria by immune cells in the formation of skin tumours. This molecular process could tip the balance between normal wound repair and tumour formation in some patients, according to researchers.

Although an association between tissue damage, chronic inflammation and cancer is well established, little is known about the underlying cause. Epidermolysis Bullosa (EB), for instance, is one of several rare inherited skin conditions associated with chronic wounding and increased risk of tumours. However, this study is the first to demonstrate that bacteria present on the skin can contribute to the development of skin tumours.

Researchers found that when mice with chronic skin inflammation are wounded they develop tumours at the wound site, with cells of the immune system required for this process to take place. They discovered that the underlying signalling mechanism involves a bacterial protein, flagellin, which is recognised by a receptor (Toll-like receptor 5) on the surface of the immune cells.

Although the direct relevance to human tumours is yet to be tested, researchers have shown that a protein called HMGB1 - found to be highly expressed in mice with chronic skin inflammation - is increased in human patients with Epidermolysis Bullosa (EB). The study found a reduction in HMGB1 levels in mice when the TLR-5 receptor was removed from immune cells. This raises the possibility of future treatments aimed at reducing levels of the flagellin bacterial protein on the skin surface, or targeting the TLR-5 receptor.